Balancing Detection and Eradication for Control of Epidemics: Sudden Oak Death in Mixed-Species Stands

Culling of infected individuals is a widely used measure for the control of several plant and animal pathogens but culling first requires detection of often cryptically-infected hosts. In this paper, we address the problem of how to allocate resources between detection and culling when the budget for disease management is limited. The results are generic but we motivate the problem for the control of a botanical epidemic in a natural ecosystem: sudden oak death in mixed evergreen forests in coastal California, in which species composition is generally dominated by a spreader species (bay laurel) and a second host species (coast live oak) that is an epidemiological dead-end in that it does not transmit infection but which is frequently a target for preservation. Using a combination of an epidemiological model for two host species with a common pathogen together with optimal control theory we address the problem of how to balance the allocation of resources for detection and epidemic control in order to preserve both host species in the ecosystem. Contrary to simple expectations our results show that an intermediate level of detection is optimal. Low levels of detection, characteristic of low effort expended on searching and detection of diseased trees, and high detection levels, exemplified by the deployment of large amounts of resources to identify diseased trees, fail to bring the epidemic under control. Importantly, we show that a slight change in the balance between the resources allocated to detection and those allocated to control may lead to drastic inefficiencies in control strategies. The results hold when quarantine is introduced to reduce the ingress of infected material into the region of interest.     

Culture of one- and two-cell bovine embryos to the blastocyst stage in the ovine oviduct

The ovine oviduct was evaluated as a culture system for early bovine embryos. One- to two-cell embryos were collected from superovulated heifers killed 36 or 48 h after the onset of estrus, embedded in agar cylinders, and transferred to oviducts ligated at the uterotubal junction. After 5 d (6.5 to 7.0 d after donor estrus), embryos were recovered and evaluated for development to the late morula or blastocyst stage. In Experiment 1, 86 embryos were cultured in 10 ewes in which the onset of estrus was synchronized with that of the donors. Fifty-eight embryos (68%) were recovered; of these, 31 (53%) had continued normal development. In Experiment 2, development in ovariectomized versus intact cyclic ewes was compared. Recovery from ovariectomized ewes (26/39, 67%) did not differ from intact cyclic ewes (26/35, 74%) and the proportion developing normally also did not differ (ovariectomized: 7/26, 27%; intact cyclic: 11/26, 42%). In Experiment 3, embryo development was compared in anestrous versus ovariectomized ewes. Recovery rate (anestrous: 22/43, 51%; ovariectomized: 20/51, 39%) and the proportion developing normally (anestrous: 8/22, 37%; ovariectomized: 9/20, 45%) did not differ between treatments. Developmental competence of oviduct-cultured embryos was tested by transfer to 16 synchronous heifers, of which eight (50%) became pregnant; five delivered calves. Results indicate that the ovine oviduct provides an adequate site for the culture of early bovine embryos.     

Purification of and production of an antibody against a 63,000 Mr stimulus-sensitive phosphoprotein in Paramecium

In vivo labeling of Paramecium cells with 32Pi most heavily labels a minor 63-kDa protein that undergoes a rapid, Ca2+-dependent dephosphorylation when the cell is stimulated to release. This stimulus-sensitive phosphoprotein was isolated and purified to apparent homogeneity. A polyclonal affinity purified antibody made against the purified protein recognizes both the phosphorylated and dephosphorylated forms of the protein. The phosphorylated 63-kDa protein is found in the cytosolic fraction; it is slightly acidic with two isoelectric forms at pI 5.8 and 6.2 and probably exists as a monomeric 60-65-kDa polypeptide in the native state. The labeled phosphoamino acid of the protein is phosphoserine. The affinity purified antibody recognizes a third isoelectric form at pI 6.3 that appears unlabeled. The specificity of the antibody was confirmed by showing that it immunoprecipitates the correct protein, i.e. the stimulus-sensitive 63-kDa phosphoprotein. The availability of purified 63-kDa protein as well as an antibody against it will now allow molecular, biochemical, and immunocytochemical studies into the role of this protein in the mechanism of exocytosis.     

Effects of Self-sown Wheat on Levels of the Take-all Disease on Seedlings of Winter Wheat Grown in a Model System

Abstract The mechanisms of build-up of inoculum of the take-all fungus, Gaeumannomyces graminis var. tritici. and infection of crop plants from self-sown (volunteer) wheat were analysed in a factorial experiment in a glasshouse. Treatments comprised sowing-date, inoculum density, soil aeration and texture, volunteer density and control of volunteers. Timing of treatments was related to field practice by the use of cumulative day-degrees and by consideration of sowing date and the geometry of seed placement. Prior sowing of volunteers, which were exposed to soil inoculum. resulted in significant increases in the incidence and severity of disease on subsequently sown seedlings. Increasing the density of volunteer seedlings increased the levels of subsequent infection. This effect, however, was significantly influenced by sowing date and density of the initial inoculum. The use of glyphosate to kill volunteers did not markedly affect the carry-over of disease.     

Modelling and Estimation of the Relative Potential for Infection of Winter Wheat by Inoculum of Gaeumannomyces graminis Derived from Propagules and Infected Roots

Abstract A model was developed to estimate the mean number of infections of seminal roots of wheat exposed to two sources of inoculum of the take-all fungus Gaeumannomyces graminis var. tritici , in an experimental system. The sources comprise discrete propagules of initial, soil inoculum and infected roots of volunteer plants that had been infected by the initial inoculum, prior to the growth of crop plants. The model was based on the probability of escape from infection by individual roots ofthe crop plants. Parameter estimation was by maximum likelihood. A model was first fitted to data for infection of roots from the soil inoculum. This yielded estimates for the efficiency of soil inoculum to cause infection in the absence of volunteer plants. The parameter for efficiency of infection by soil inoculum was resolved into components for inoculum density, survival of inoculum and the probability of success of individual propagules. The model was extended to include simultaneous exposure of crop roots to soil inoculum and to root inoculum on the volunteer plants. The presence of volunteer seedlings prior to sowing of crop plants resulted in an increase in the effectiveness of inoculum to cause disease. Sowing date and soil condition, as affected by addition of sand, were shown to have significant effects on the efficiency of both sources of inoculum.     

Calmodulin antagonists inhibit secretion in Paramecium

Secretion in Paramecium is Ca2+-dependent and involves exocytic release of the content of the secretory organelle, known as the trichocyst. The content, called the trichocyst matrix, undergoes a Ca2+-induced reordering of its paracrystalline structure during release, and we have defined three stages in this expansion process. The stage I, or fully condensed trichocyst, is the 4 microns-long membrane-bounded form existing prior to stimulation. Stage II, the partially expanded trichocyst, we define as an intermediate stage in the transition, preceding stage III, the fully expanded extruded form which is a 20-40 microns-long needlelike structure. These stages have been used to assay the effects of trifluoperazine (TFP) and W-7, calmodulin (CaM) antagonists, on trichocyst matrix expansion in vivo. TFP and W-7 are shown to reversibly block matrix release induced by picric acid. Ultra-structural examination reveals that one effect of this inhibition is reflected in the organelles themselves, which are prevented from undergoing the stage I-stage II transition by preincubation in 14 microM TFP or 35 microM W-7 before fixation. This inhibition of expansion by TFP can be moderated but not abolished by high extracellular Ca2+ (5 mM). The moderation by high Ca2+ can be eliminated by raising TFP concentration to 20 microM. A possible explanation for the ability to titrate the inhibition in this manner is that TFP is acting to block expansion by binding to the Ca2+-CaM complex. Brief exposure of cells to the Ca2+ ionophore A23187 and 5 mM Ca2+ following TFP treatment promotes matrix expansion, although in 14 microM TFP a residual level of inhibition remains. These results suggest that, following stimulation, CaM regulates secretion in Paramecium, possibly by controlling the Ca2+-dependent matrix expansion which accompanies exocytosis in these cells.     

A major difference between the divergence patterns within the lines-1 families in mice and voles

L1 retroposons are represented in mice by subfamilies of interspersed sequences of varied abundance. Previous analyses have indicated that subfamilies are generated by duplicative transposition of a small number of members of the L1 family, the progeny of which then become a major component of the murine L1 population, and are not due to any active processes generating homology within preexisting groups of elements in a particular species. In mice, more than a third of the L1 elements belong to a clade that became active approximately 5 Mya and whose elements are > or = 95% identical. We have collected sequence information from 13 L1 elements isolated from two species of voles (Rodentia: Microtinae: Microtus and Arvicola) and have found that divergence within the vole L1 population is quite different from that in mice, in that there is no abundant subfamily of homologous elements. Individual L1 elements from voles are very divergent from one another and belong to a clade that began a period of elevated duplicative transposition approximately 13 Mya. Sequence analyses of portions of these divergent L1 elements (approximately 250 bp each) gave no evidence for concerted evolution having acted on the vole L1 elements since the split of the two vole lineages approximately 3.5 Mya; that is, the observed interspecific divergence (6.7%-24.7%) is not larger than the intraspecific divergence (7.9%-27.2%), and phylogenetic analyses showed no clustering into Arvicola and Microtus clades.      

Scaling and spatial dynamics in plant-pathogen systems: from individuals to populations

Components of transmission for primary infection from soil-borne inoculum and secondary (plant to plant) infection are estimated from experiments involving single plants. The results from these individual-based experiments are used in a probabilistic spatial contact process (cellular automaton) to predict the progress of an epidemic. The model accounts for spatial correlations between infected and susceptible plants due to inhomogeneous mixing caused by restricted movement of the pathogen in soil. It also integrates nonlinearities in infection, including small stochastic differences in primary infection that become amplified by secondary infection. The model predicts both the mean and the variance of the infection dynamics of R. solani when compared with replicated epidemics in populations of plants grown in microcosms. The broader consequences of the combination of experimental and modelling approaches for scaling-up from individual to population behaviour are discussed. <br>